Langhans-type more than foreign body-type multinucleated giant cells are induced from UVB-irradiated monocytes.
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Adult↗
Biomedical subjects
Kana Mizuno
Publications and source records attributed to Kana Mizuno.
Ultraviolet B radiation suppresses endocytosis, subsequent maturation, and migration activity of langerhans cell-like dendritic cells.
Langerhans cells capture exogenous antigens through fluid phase pinocytosis and receptor-mediated endocytosis and migrate to lymph nodes, where they present processed antigen to T cells. Ultraviolet B radiation impairs the antigen-presenting function of Langerhans cells, resulting in antigen-specific immunosuppression of contact hypersensitivity. We tested the notion that ultraviolet B radiation inhibits the endocytic activity of Langerhans cells, leading to impaired migration and maturation. Human monocyte-derived Langerhans cell-like dendritic cells that took up lucifer yellow or fluorescein isothiocyanate dextran exclusively migrated in response to 6Ckine/secondary lymphoid chemokine, and matured, as evidenced by an increase in CD54 and CD86 expression and potent stimulatory activity in allogeneic mixed lymphocyte reaction. Exposing Langerhans cell-like dendritic cells to 20-40 mJ per cm2 of ultraviolet B radiation reduced their endocytic activity in fluid phase pinocytosis (measured by uptake of lucifer yellow) and in receptor-mediated endocytosis (measured by uptake of fluorescein isothiocyanate dextran). Membrane ruffling and CD32 expression were also suppressed by ultraviolet B radiation. Ultraviolet B-irradiated, endocytosing Langerhans cell-like dendritic cells had less movement towards 6Ckine, expressed less CD54 and CD86, and had less effective stimulatory activity in allogeneic mixed lymphocyte reaction than nonirradiated, endocytosing Langerhans cell-like dendritic cells. Endocytosis upregulated tumor necrosis factor alpha production by Langerhans cell-like dendritic cells, but prior ultraviolet B radiation inhibited this enhancement. These data suggested that impaired endocytosis and subsequent inhibitory migration and maturation of Langerhans cells by ultraviolet B radiation could contribute to local immunosuppression of contact hypersensitivity.
Adult↗
[Human monocyte-derived multinucleated giant cells].
Multinucleated giant cells (MGC) are characteristic cells in granulomatous disorders such as sarcoidosis and leprosy. There are two types of MGC; foreign body-type and Langhans-type cells. The exact mechanisms of the formation and the functional significance of MGC are not determined, although their morphological features are well understood. MGC are also formed in vitro from peripheral blood mononuclear cells by stimulation with cytokines and lectins. Particularly IFN-gamma is considered to play a pivotal role in monocyte fusion. IL-3, IL-4, IL-13, and GM-CSF are other reported cytokines involved in MGC formation. In addition to such inflammatory mediators, a factor derived from the pathogens of granulomatous disorders may be necessary for MGC formation. Muramyl dipeptide, a peptidoglycan portion of bacterial cell walls, is one of the candidates and can preferentially induce Langhans-type cells in in vitro MGC formation system. Although the exact mechanisms of in vitro MGC formation remains unknown, cell surface molecules such as P2X7 receptor, integrins, CD98, and macrophage fusion protein are considered to be involved in fusion process. Monocytes of sarcoidosis patients expressed higher levels of P2X7 and had a higher ability to induce MGC than those of healthy controls. Effective agents for sarcoidosis such as tranilast, alloprinol, and captopril inhibited in vitro MGC formation, suggesting their therapeutic effects through the direct effects on monocytes. Thus, an in vitro MGC formation model would be a useful tool to understand the relevance of MGC in granulomatous disorders.
Acetylmuramyl-Alanyl-Isoglutamine↗
Monocyte-derived multinucleated giant cells and sarcoidosis.
Multinucleated giant cells (MGC) are characteristic cells in granulomatous disorders such as sarcoidosis and also formed in vitro from peripheral blood mononuclear cells by stimulation with cytokines, including interferon-gamma (IFN-gamma), interleukin-3 (IL-3), IL-4, IL-13, and granulocyte-macrophage-colony stimulating factor. In addition to such inflammatory mediators, a factor derived from the pathogens of granulomatous disorders may be necessary for MGC formation. Muramyl dipeptide (MDP), a peptidoglycan portion of bacterial cell walls present in sarcoidal lesions, is one of the candidates and can preferentially induce Langhans-type cells (LGC) in in vitro MGC formation system. Although the exact mechanisms of in vitro MGC formation remains unknown, receptors such as P2X(7), integrins, CD98, and macrophage fusion protein are considered to be involved in cell-to-cell adhesion and subsequent fusion process. Monocytes from sarcoidosis patients expressed higher levels of P2X(7) and had a higher ability to induce MGC than those from healthy controls. Attributable cells for the formation were CD14(++)CD16(-) monocytes. Therefore, CD14(++)CD16(-) monocytes may infiltrate into sarcoidal lesions and be fused to form LGC by inflammatory mediators and MDP derived from the pathogens of the disorder. Effective agents for sarcoidosis such as tranilast, allopurinol, and captopril inhibited in vitro MGC formation through inhibiting the expression of adhesion molecule and purinergic receptor. Thus, an in vitro MGC formation model would be a useful tool to understand the relevance of MGC in granulomatous disorders.
Giant Cells↗
Langhans-type and foreign-body-type multinucleated giant cells in cutaneous lesions of sarcoidosis.
Multinucleated giant cells are characteristic of a monocyte-macrophage lineage in sarcoidosis and consist of two types of cells: Langhans-type with an arcuate arrangement of nuclei and a foreign-body type with random arrangement of nuclei. To compare these cells in the cutaneous lesions of sarcoidosis, we histologically and immunohistologically examined multinucleated giant cells in 25 scar infiltrations (cutaneous sarcoidosis with foreign bodies) and 30 cutaneous lesions of sarcoidosis without foreign bodies. Regardless of the presence or absence of foreign bodies, the cutaneous lesions had both types of multinucleated giant cells, usually with a predominance of the Langhans-type, although the numbers of total multinucleated giant cells were higher in scar infiltrations than in cutaneous sarcoidosis without foreign bodies, suggesting that their frequency is influenced by the microenvironment in sarcoidal lesions such as the presence of foreign bodies. Immunohistochemical studies using surface antigens of monocyte-macrophage lineage cells and adhesion molecules indicated that both types of multinucleated giant cells are formed from monocytes rather than tissue macrophages and are phenotypically the same cells with different distributions of nuclei.
Giant Cells, Foreign-Body↗
Circulating CD14+ CD16+ monocytes are expanded in sarcoidosis patients.
Sarcoidosis is a systemic disease of unknown etiology characterized by noncaseating granulomas, consisting mainly of epithelioid cells and multinucleated giant cells derived from monocyte-macrophage lineage cells. Monocytes fall into subpopulations comprising CD14++ CD16-, and CD14+ CD16+ cells, and expansion of the later monocytes has been reported under some pathological conditions. In this study, we examined the immunophenotype of blood monocytes in patients with sarcoidosis using two-color immunofluorescence flow cytometry. In healthy controls CD14+ CD16+ monocytes account for 5.8 +/- 2.8% of monocytes. The percentage of CD14+ CD16+ monocytes was significantly higher (p <0.02) in the sarcoidosis patients (11.8 +/- 4.9%) compared with those in healthy control subjects. The serum ACE levels were significantly correlated with the percentage of CD14+ CD16+ monocytes (p <0.05). In contrast, the percentage was not correlated with purinergic receptor expression of monocytes as estimated by LDH release from BzATP-stimulated monocytes. These findings suggest that CD14+ CD16+ monocytes represent a sensitive marker for the disease activity of sarcoidosis.
Adult↗